Abstract
Commentary on SSO and other putative inhibitors of FA transport across membranes by CD36 disrupt intracellular metabolism, but do not affect fatty acid translocation
Highlights
Long-chain fatty acid (LCFA) transport is fundamental to human pathophysiology, and its impairment has been implicated in cardiovascular disease, cancer, and obesitylinked diabetes [1,2,3,4]
The ongoing search for the LCFA translocation mechanisms was influenced by a precedent: glucose transport! Because it has many hydroxyl groups, glucose is insoluble in hydrocarbons and does not spontaneously translocate across the plasma membrane
CD36 is localized to the plasma membrane outer leaflet, and the mechanism by which it transfers LCFA to the inner leaflet adjacent to the cytoplasm is unknown
Summary
Long-chain fatty acid (LCFA) transport is fundamental to human pathophysiology, and its impairment has been implicated in cardiovascular disease, cancer, and obesitylinked diabetes [1,2,3,4]. How LCFAs transfer between lipid surfaces separated by an aqueous phase is largely uncontroversial; LCFAs enter cells by diffusion to and insertion into the outer leaflet, translocation to the inner leaflet, and desorption into the cytoplasm. According to the principle of microscopic reversibility, the mechanisms for insertion (kon) and desorption (koff) are the same [8], so that the reverse process (kon), occurs by LCFA insertion into a membrane leaflet acyl chain first, followed by desorption of the anionic, charged form [9].
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